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Aspirin's Preventive Colon Cancer Effect Depends On Genes

Taking a daily dose of aspirin helps lower the risk of colon cancer. However, a new study has found that the reduced risk of colorectal cancer is affected by a mutation of a gene called BRAF.

Colon cancer is a leading cause of cancer-related death worldwide. In 2008, there were 1.23 million new clinically diagnosed cases of colorectal cancer; over 608,000 people died from the disease that year.

The study, published in JAMA, identified that the association between daily aspirin use and reduced risk of colon cancer depends on specific gene mutations.

Data was collected from 2 large studies, the Nurses' Health Study and the Health Professionals Follow-Up Study, which included over 127,000 people.

The researchers, led by Reiko Nishihara of the Dana-Farber Cancer Institute in Boston, found that those who were at a reduced risk of developing colon cancer had the "typical", wild-type, form of the BRAF gene. Regular aspirin use lowered the risk of developing BRAF-wild-type cancer by 27 percent.

However, those who had the mutated form of BRAF didn't benefit at all.

The finding suggests that colon tumor cells with the BRAF mutation are much less sensitive to the beneficial effects of aspirin,.

The authors said that "the association of aspirin use with colorectal cancer risk differed significantly according to BRAF mutation status."

In addition, the investigators found people were at a lower risk of BRAF-wild-type cancer the more aspirin tablets they took each week.

The authors said that there was "no statistically significant interaction between post-diagnosis aspirin use and BRAF mutation status in colorectal cancer-specific or overall survival analysis."

The finding suggests that the protective effects associated with aspirin use differ by BRAF status at early stages of tumor evolution, but not at later phases.

They authors said:

"The identification of specific cancer-subtypes that are prevented by aspirin is important for several reasons. First, it enhances our understanding of the molecular pathogenesis of colorectal neoplasia and the mechanisms through which aspirin may exert its antineoplastic effects.

Second, development of clinical, genetic, or molecular predictors of specific subtypes of colorectal cancer might lead to the development of more tailored screening or chemo-preventive strategies.

They concluded:

Nevertheless, given the modest absolute risk difference, further investigations are necessary to evaluate clinical implications of our findings. Lastly, our data provide additional support for a causal association between aspirin use and risk reduction for a specific subtype of colorectal cancers. Accumulating evidence supports preventive effect of aspirin against colorectal cancer."

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